Search PubMed⌕ Search

Biomedical subjects

A A Bove

Publications and source records attributed to A A Bove.

At least 19 recordsLinked to original sources
PubMed1992

Comparison of angiographic center and local site analysis of PTCA results in a multicenter angioplasty-restenosis trial. The M Heart Group.

We compared three methods of coronary stenosis (S) sizing in a multihospital PTCA restenosis trial: visual analysis by independent observers, single point caliper measurements, and quantitative coronary angiography (QCA). Cine films from 50 patients were submitted from the clinical site to the quantitative angiographic center, where visual analysis and computer quantitation were performed. Regression analysis revealed a correlation coefficient of .857 for caliper vs. QCA (p less than .0001) and .876 for visual observation vs. QCA (p less than .0001). No significant differences were found between any of the 3 methods for pre- or post-PTCA stenosis values. However, QCA yielded smaller PTCA changes in stenosis severity than either caliper or visual observation (p less than .05). Both caliper and visual methods correlated well with QCA in assessing stenosis size pre- and post-PTCA. Trained observers can visually assess lesion severity with accuracy approaching QCA. QCA is likely to be less expensive when compared to visual analysis by three experienced observers and should be the method used for estimating the results of PTCA in clinical trials.

Adrenal Cortex Hormones↗
PubMed1991

Exercise-induced increases in atrial natriuretic factor are attenuated by endurance training.

Short-term exercise has been associated with increased plasma levels of atrial natriuretic factor, a potent dilating and natriuretic hormone. In this study, the effect of exercise training on atrial natriuretic factor release during short-term exercise was investigated in men without a history of cardiovascular or other major disease. A well trained group of 10 men who exercised an average of 6,618 kcal/week was compared with a minimally trained group of 9 men who exercised 1,479 kcal/week. Maximal oxygen uptake was 55.2 ml/kg per min in the well trained group and 42.5 ml/kg per min in the minimally trained group (p less than 0.05). Plasma for atrial natriuretic factor, norepinephrine and epinephrine was obtained at rest, at 4 min of exercise and at maximal exercise. Atrial natriuretic factor was lower at rest in the minimally trained than in the well trained men (23 vs. 35.9 pg/ml, p less than 0.05). At maximal exercise, atrial natriuretic factor increased 2.6 times the value at rest in minimally trained men (59.8 pg/ml, p less than 0.05 vs. rest), but did not change in well trained men (34 pg/ml). In minimally trained men at rest, at 4 min of exercise and at maximal exercise, plasma levels of atrial natriuretic factor correlated with heart rate, cardiac output, mean arterial pressure and plasma levels of norepinephrine and epinephrine; these correlations were not found in the well trained group. Thus, short-term exercise results in a significant increase in atrial natriuretic factor in minimally trained but not in well trained men.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Intravenous cocaine causes epicardial coronary vasoconstriction in the intact dog.

The effect of intravenous cocaine on coronary artery dynamics in 23 closed-chest dogs was examined. To determine dose-related effects, intravenous cocaine was administered in doses of 1, 3, 6, and 9 mg/kg; saline solution was used in control dogs. Heart rate, aortic pressure, and left anterior descending coronary artery cross-sectional area were measured before and for 60 minutes after each injection. Myocardial blood flow was measured with 15 microns radioactive microspheres at baseline and 30 minutes after administration of cocaine or saline solution. Plasma cocaine, benzoyl ecgonine, and norepinephrine concentrations were measured and correlated with physiologic changes. Cocaine caused sustained dose-dependent vasoconstriction of the left anterior descending coronary artery, which was significant at 15 minutes and maximum at 60 minutes (control = 2 +/- 10%; cocaine, 9 mg/kg = 46 +/- 10% cross-sectional area reduction). There was an immediate but transient reduction in aortic pressure and an elevation of heart rate after the 6 and 9 mg/kg doses and no hemodynamic changes with lower doses. Coronary blood flow was reduced 30 minutes after the 3, 6, and 9 mg/kg doses. Two dogs had refractory ventricular tachycardia after injection of cocaine and were not included in the analysis. Results of this investigation demonstrate angiographic evidence of dose-dependent, cocaine-induced epicardial coronary vasoconstriction and deleterious hemodynamic abnormalities at commonly used doses of cocaine. These results demonstrate a mechanism for the development of angina and myocardial infarction associated with cocaine use.

Animals↗
PubMed1991

Multi-Hospital Eastern Atlantic Restenosis Trial. II: A placebo-controlled trial of thromboxane blockade in the prevention of restenosis following coronary angioplasty.

Since platelet interactions appear to play an important role in the development of restenosis, attenuation of thromboxane-mediated reactions may improve the long-term outcome following coronary angioplasty. Phase II of the Multi-Hospital Eastern Atlantic Restenosis Trial (M-HEART) is a prospective, randomized, placebo-controlled study of thromboxane blockade in the prevention of restenosis following successful coronary angioplasty. Two forms of thromboxane blockade are evaluated: aspirin (a nonspecific inhibitor of thromboxane synthesis) and sulotroban (a specific thromboxane receptor antagonist). The design of this multicenter trial and the rationale for use of sulotroban in the prevention of restenosis are reviewed in this report.

Angioplasty, Balloon, Coronary↗
PubMed1991

Complexes of .NO with nucleophiles as agents for the controlled biological release of nitric oxide. Vasorelaxant effects.

Selected nucleophile/nitric oxide adducts [compounds which contain the anionic moiety, XN(O-)N = O] were studied for their ability to release nitric oxide spontaneously in aqueous solution and for possible vasoactivity. The diversity of structures chosen included those in which the nucleophile residue, X, was that of a secondary amine [Et2N, as in [Et2NN(N = O)O]Na, 1], a primary amine [iPrHN, as in [iPrHNN(N = O)O]Na, 2], a polyamine, spermine [as in the zwitterion H2N(CH2)3NH2+(CH2)4N[N(N = O)O-](CH2)3NH2, 3], oxide [as in Na[ON(N = O)O]Na, 4], and sulfite [as in NH4[O3SN(N = O)O]NH4, 5]. The rate constants (k) for decomposition in pH 7.4 phosphate buffer at 37 degrees C, as measured by following loss of chromophore at 230-260 nm, were as follows: 1, 5.4 x 10(-3) s-1; 2, 5.1 x 10(-3) s-1; 3, 0.30 x 10(-3) s-1; 4, 5.0 x 10(-3) s-1; and 5, 1.7 x 10(-3) s-1. The corresponding extents of nitric oxide release (ENO) were 1.5, 0.73, 1.9, 0.54, and 0.001 mol/mol of starting material consumed, respectively, as determined from the integrated chemiluminescence response. Vasodilatory activities expressed as the concentrations required to induce 50% relaxation in norepinephrine-constricted aortic rings bathed in pH 7.4 buffer at 37 degrees C (EC50) were as follows: 1, 0.19 microM; 2, 0.45 microM; 3, 6.2 microM; 4, 0.59 microM; and 5, 62 microM. Vasorelaxant potency (expressed as 1/EC50) was strongly correlated with the quantity of .NO calculated from the physicochemical data to be released in the interval required to achieve maximum relaxation at the EC50 doses (r = 0.995). This suggests that such nucleophile/.NO adducts might generally be useful as vehicles for the nonenzymatic generation of nitric oxide, in predictable amounts and at predictable rates, for biological purposes. The particular significance for possible drug design is underscored in the very favorable potency comparison between several of these agents and the established nitrovasodilators sodium nitroprusside and glyceryl trinitrate (EC50 values of 2.0 and greater than 10 microM, respectively) in parallel aortic ring tests.

Animals↗
PubMed1991

Importance of endothelial function in stenotic haemodynamic responses.

STUDY OBJECTIVE: The aim was to examine endothelium mediated flow dependence in a dynamic stenosis. DESIGN: The coronary circulation was modelled as a proximal compliant stenosis and a fixed distal resistance. Pressures and flow were calculated using standard haemodynamic equations. Within the stenosis, the vessel wall was composed of normal and rigid sections, and the normal section dilated proportionally with flow. From this theoretical analysis, three perfusion pressures (150, 100, and 75 mm Hg) and two distal resistances (high and low) were examined. MAIN RESULTS: In a stenotic artery (93% area reduction) with high flow dependence, decreasing distal resistance increased flow substantially. At 75 mm Hg perfusion pressure, flow increased from 40.8 to 81.6 ml.min-1. With moderate flow dependence, flow increases were attenuated. Without flow dependence, flow increases were smaller, and at low perfusion pressure, flow paradoxically decreased (39.0 to 0.0 ml.min-1) when distal resistance decreased. Vasoconstriction responses with and without flow dependence were analysed. In a stenotic artery, vasoconstrictors caused a concentration dependent decrease in flow. Without flow dependence, the flow dose-response curve was shifted to the left: a lower level of arterial vasoconstriction resulted in a greater flow decrease. CONCLUSIONS: The theoretical analysis shows significantly different flow responses to decreasing distal resistance and to vasoconstriction depending on endothelial function. Endothelial dysfunction may be important in the pathophysiology of angina pectoris.

Arterial Occlusive Diseases↗
PubMed1991

Exercise training and responsiveness of isolated coronary arteries.

Exercise is associated with release of catecholamines and vasoactive intestinal polypeptides. Recurrent exposure to catecholamines modifies the sensitivity of adrenoceptors. To test the hypothesis that exercise training may affect the sensitivity of the epicardial coronary arteries, we performed studies on isolated coronary arteries from male dogs capable of running on a treadmill. The animals were separated randomly into two groups: sedentary and exercise training. After 11 wk, rings of left circumflex and left anterior descending coronary arteries were studied in vitro. Contractions to alpha 1-adrenergic agonists (norepinephrine and phenylephrine) were not affected by exercise training. During contractions with prostaglandin F2 alpha, endothelium-dependent relaxations to alpha 2-adrenergic agonists (norepinephrine and UK 14304) were not reduced significantly by exercise training. The concentration-relaxation curves to beta-adrenergic agonists (norepinephrine, isoproterenol, and epinephrine) were shifted to the right after training. The concentration-response curves to vasoactive intestinal polypeptide, but not that to substance P, were shifted to the right in rings with endothelium from exercise-trained animals. These findings demonstrate a decrease in responsiveness of canine vascular smooth muscle to beta-adrenergic agonists and to vasoactive intestinal polypeptide after exercise training.

Animals↗
PubMed1991

Catecholamine metabolic pathways and exercise training. Plasma and urine catecholamines, metabolic enzymes, and chromogranin-A.

BACKGROUND: Because acute exercise increases systemic catecholamines, we sought to determine whether exercise training would alter daily or exercise-related catecholamine release and inactivation. METHODS AND RESULTS: In 24-hour urine collections, catecholamines and metabolites provided indexes of overall oxidative deamination, sulfation, and O-methylation. Plasma catecholamines, the sulfoconjugates of each, and chromogranin-A were determined at rest and during exercise in 10 well-trained male subjects and nine minimally trained male subjects (maximal oxygen uptake 55.2 and 42.5 ml/kg/min, respectively), and levels of activities of catechol-O-methyltransferase (COMT), monoamine oxidase B (MAO-B), and thermolabile phenolsulfotransferase (TL-PST) were also determined. Plasma-free catecholamines showed minimal differences between the two groups at submaximal exercise (4 minutes) but large differences at maximal exercise, reflecting the different exercise levels attained. Inactivation of plasma catecholamines by sulfation across rest and exercise tended to be greater in the well-trained group, with small increases in both plasma sulfoconjugated dopamine and sulfoconjugated norepinephrine. In the well-trained group, urinary metabolites demonstrated trends toward increased dopamine release (p less than 0.07) and small increases in the daily release of epinephrine and its sulfoconjugated metabolites. Indexes of deamination, sulfoconjugation, and O-methylation, with the exception of a reduced deamination of dopamine and the activities of COMT, MAO-B, and TL-PST were not different in the two groups. CONCLUSIONS: Despite considerable differences in the exercise activities per week between well-trained and minimally trained individuals, there were minimal differences in the release and metabolism of catecholamines at rest or during exercise.

Adult↗
PubMed1990

Detection of mild coronary stenoses using the Dynamic Spatial Reconstructor.

The accuracy of the Dynamic Spatial Reconstructor (DSR) in the detection of moderate coronary artery stenoses was examined in 20 closed-chest dogs. Twenty-eight hollow plastic cylinders were embolized into the left coronary arteries and produced 25% to 56% reductions in arterial lumina diameter. For each dog, one three-dimensional (3-D) image of the heart was reconstructed from each DSR scan recorded during injection of contrast into the aortic root. Analysis involved blinded visual analysis by four independent observers of multiview projection images computed from the single 3-D image. Postmortem coronary angiograms of the isolated heart were considered definitive for location of the stenoses. Overall sensitivity of detection by DSR was 89% and specificity 81%. Sensitivity of detecting stenoses greater than or equal to 50% was 98%. Receiver operating characteristics (ROC) analysis showed that detection of stenoses in the left coronary arteries is of equal sensitivity and specificity.

Animals↗
PubMed1990

What stimulates atrial natriuretic factor release during exercise?

Prior studies have shown that circulating atrial natriuretic factor (ANF) increases during short-term exercise, but the mechanism controlling ANF release, as well as the effect of exercise training on ANF release, remains unclear. Fifteen healthy mongrel dogs underwent short-term exercise testing before and after a 12-week period of exercise training (n = 8) or cage confinement (n = 7). ANF, norepinephrine, epinephrine, right atrial pressure, and heart rate were measured simultaneously at rest and during exercise at the time of each acute exercise study. Data were analyzed for all animals with normal baseline ANF values. Exercise training had no modulating effect on circulating ANF levels at rest or during exercise. Therefore, data before and after exercise training or cage confinement were grouped (n = 24) to determine the effects of short-term exercise. ANF levels increased from 49 +/- 2 pg/ml at rest to 60 +/- 4 pg/ml during exercise (p less than 0.05). Heart rate, norepinephrine, and epinephrine values also increased, but right atrial pressure actually decreased from 2.3 +/- 0.9 mm Hg at rest to -3.8 +/- 0.9 mm Hg during exercise (p less than 0.05). There was no correlation between ANF concentrations and levels of these other variables either at rest of during exercise. By demonstrating an increase in ANF with a simultaneous decrease in right atrial pressure, this study clearly shows that increased right atrial pressure is not the secretory stimulus for ANF release during exercise in the normal dog. The lack of correlation between ANF and right atrial pressure, heart rate, norepinephrine, and epinephrine levels suggests that factors other than these variables stimulate ANF release during short-term exercise.

Animals↗
PubMed1990

Combined arterial gas embolism and decompression sickness following no-stop dives.

Decompression sickness (DCS) has been clinically classified as Type I (predominantly joint pain) or Type II (predominantly spinal cord lesions). We present 3 cases that are all characterized by severe (Type II) DCS with signs and symptoms of spinal cord injury occurring in conjunction with arterial gas embolism (AGE). We consider the AGE "minor" because only 2 of the 3 subjects initially lost consciousness, and in all cases the signs and symptoms of the AGE had essentially resolved within 1 h or by the time recompression therapy began. DCS was resistant to recompression therapy, even though treatment began promptly after the accident in 2 of the 3 cases. None of the cases had a good neurologic outcome and there has been one death. None of the divers exceeded the U.S. Navy "no-stop" limits for the depths at which they were diving. We have observed a previously unreported clinical syndrome characterized by severe Type II DCS subsequent to AGE following pressure-time exposures that would normally not be expected to produce DCS. We postulate that AGE may have precipitated or predisposed to this form of DCS.

Adult↗
PubMed1989

Inhibition of platelet and red blood cell accumulation on damaged arterial surfaces with albumin pretreatment.

Damaged arterial surfaces initiate platelet accumulation which leads to thrombus formation. On artificial surfaces, albumin pretreatment inhibits platelet deposition. To investigate albumin pretreatment on damaged vessel surfaces, 16 carotid arteries were obtained from 8 anesthetized dogs (11-15 kg). Each artery was divided into 2 segments. Each segment was mounted in a perfusion system, distended to 100 mmHg, and the middle section damaged. One segment was perfused with Tyrodes solution plus bovine albumin (5 g/100 ml), while the other segment was perfused only with Tyrodes solution. After 120 mins, both segments were perfused with whole citrated blood containing Indium-111 labeled platelets. Without albumin pretreatment, the proximal section contained 11 +/- 8 (X +/- SEM) percent of total blood radioactivity, while the damaged section contained 53 +/- 11 percent (p less than 0.01). Albumin pretreatment significantly reduced platelet deposition in the damaged section (53 +/- 11 versus 9 +/- 6 percent, p less than 0.01). Further, with albumin pretreatment the radioactive counts in the damaged section were not significantly different from the nondamaged proximal section (9 +/- 6 vs 8 +/- 7 percent, p greater than .8). Quantitative examination of the scanning electron micrographs demonstrated significantly more platelet and red blood cell coverage of the damaged segments (60 +/- 12.8 percent) than of the albumin treated segments (12.9 +/- 5 percent). In four additional experiments, we pretreated arterial segments with albumin for varying time intervals. After 15, 30 and 60 mins of albumin pretreatment, each artery was perfused with radiolabeled platelets and whole blood for 5 mins at 100 mmHg perfusion pressure. Radioactive evidence of platelet deposition on arterial segments treated with albumin for 15, 30, and 60 minutes was also significantly less than control (p less than .05). Beneficial effects of albumin were apparent up to 30 mins of blood flow at 100 mm Hg. Our results suggest that albumin may inhibit platelet and red blood cell deposition on damaged arteries. This could be an adjunct therapy for vessel preservation during artery bypass procedures.

Albumins↗
PubMed1989

Gender-related differences in cardiac response to supine exercise assessed by radionuclide angiography.

This study examines the recently reported gender differences in cardiac responses to exercise. The study group consisted of 192 men and 67 women with a low probability of coronary artery disease who underwent supine exercise radionuclide angiography. Men had a lower rest ejection fraction than that of women (0.63 versus 0.66, p = 0.02) and greater increases in ejection fraction with exercise (0.08 versus 0.02, p = 0.0001). The slope relating ejection fraction to metabolic equivalents of exercise (METs) was greater (p = 0.004) for men, even after adjustment for differences in rest ejection fraction and end-diastolic volume index. Compared with men, women had a smaller rest end-diastolic volume index (87 versus 97 ml/m2, p = 0.003) and a greater increase in end-diastolic volume index with exercise (6 versus -2 ml/m2, p = 0.002). The slope relating end-diastolic volume to METs was greater for women, even after adjustment for differences in rest end-diastolic volume index and peak work load. There are clear gender differences in the supine exercise response of ejection fraction and end-diastolic volume that are not explained by differences in exercise capacity.

Adult↗
PubMed1989

Complement activation from protamine sulfate administration after coronary angiography.

The cause of hypotension after reversal of heparin by protamine has not been well defined. In this study we evaluated complement activation (C3a and C4a) by the heparin-protamine complex in 46 consecutive patients (40 received protamine sulfate to reverse heparin, and six did not) during and after coronary angiography. In patients receiving protamine sulfate, there was a significant increase in C3a over the value before protamine sulfate administration (P less than .001) or in patients who did not receive protamine sulfate (P less than .05): 807 +/- 100 ng/ml vs. 274 +/- 75 ng/ml. There were no significant changes in C4a after protamine sulfate administration. These results indicate that the alternate complement pathway is activated when protamine sulfate is administered after coronary angiography. This may induce hypotension as well as platelet aggregation and thrombus formation and may contribute to coronary instability. Therefore, in unstable patients, heparin reversal by protamine should not be done routinely.

Anaphylatoxins↗
PubMed1989

Weighted ventriculographic wall motion score for improved survival prediction in patients with coronary artery disease. Coronary Artery Surgery Study.

Global ventricular function parameters such as the ejection fraction and the sum of wall motion scores for segments of the left ventricle are excellent predictors of long-term survival in patients with coronary heart disease. These are usually determined from a monoplane right anterior oblique view. It was hypothesized that a biplane weighted wall motion score that included the left anterior oblique projection might better predict survival. A new score (BISCORE) was derived for 1,433 Mayo Clinic ventriculograms coded by the methods of the Coronary Artery Surgery Study (CASS). Weighting coefficients for each left ventricular segment were derived by the proportional hazards technique, and this resulted in the equation BISCORE = 120 - (8.6 x anterobasal + 3.4 x basal septum + 2.9 x apical + 2.7 x posterolateral + 2.4 diaphragmatic), which yielded a score from 0 (all segments aneurysmal) to 100 (all segments normal). This score stratified the original 1,433 patients into distinct groups by survival. As a single variable it was better than previous wall motion scores and ejection fraction at predicting survival. When prospectively applied to 5,172 Coronary Artery Surgery Study patients, this new score again proved to be a better predictor of survival than previous unweighted scores. Since the new score contains terms from the left anterior oblique ventriculographic projection, it is concluded that this projection adds information to that of the right anterior oblique projection regarding survival. Furthermore, this weighted score appears more highly associated with survival than unweighted scores.

Coronary Disease↗
PubMed1989

Epicardial coronary artery constriction with intravenous ethanol.

Although in vitro studies have demonstrated ethanol-induced coronary artery constriction, in vivo reports suggest an ethanol-related coronary dilator effect with increases in coronary blood flow. The principal difference in these studies is the demonstration of epicardial coronary constriction with ethanol, while dilation is described only in resistance vessels. Clinical studies have noted evidence of myocardial ischemia following ethanol ingestion in patients with coronary artery disease, suggesting ethanol-related constriction of diseased epicardial coronary arteries. This study hypothesized that intravenous ethanol would constrict canine epicardial coronary arteries while producing arteriolar resistance vessel dilatation. Ten closed-chest mongrel dogs weighing 24 +/- 1 kg (mean +/- SEM) were given 8 g of ethanol intravenously over 30 min. Left anterior descending and circumflex proximal artery diameters were measured by quantitative coronary angiography; myocardial flow was measured by Xenon washout, and myocardial flow distribution was measured with radioactive microspheres. Baseline proximal left anterior descending and circumflex artery areas were 6.3 +/- 0.5 and 5.8 +/- 0.4 mm2, respectively. Up to 30% left anterior descending and circumflex proximal artery narrowing was noted at 60 and 90 min following ethanol infusion. The constriction was reversed with nitroglycerin. There was a decrease in left anterior descending artery flow but no change in circumflex artery flow at 60 min. Blood ethanol level varied from 520 micrograms/ml initially to 205 micrograms/ml 90 min after the infusion terminated (intoxication = 1500 micrograms/ml). These data suggest that ethanol has significant vasoconstrictor action in vivo on epicardial coronary arteries.

Alcoholism↗
PubMed1989

Left main coronary artery disease: radionuclide angiographic function versus anatomic correlates with visual and quantitative angiographic methods.

The results of exercise radionuclide angiography in 29 patients with significant left main coronary artery stenosis were examined to correlate functional left ventricular performance with anatomic severity of left main coronary artery stenosis. Change in ejection fraction, regional wall motion, and peak ejection fraction were widely variable; none of these parameters correlated with severity of left main stenosis as assessed by visual or quantitative angiographic methods. Twenty-five patients (86%) had two or more of the following indicators of ischemia with exercise: chest pain, significant ST-segment depression, systolic hypotension, definite decrease in ejection fraction, or definite decline in regional wall motion. However, four patients (14%) had only mild abnormalities in ejection fraction and regional wall motion, although they did have hemodynamic and electrocardiographic evidence of severe ischemia. Exercise radionuclide angiography yields heterogeneous results in patients with significant left main coronary artery stenosis. Anatomically severe left main coronary artery stenosis is not always associated with mechanical evidence of severe ischemia.

Adult↗